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In November 1906, Alois Alzheimer, a German psychiatrist presented the clinical features of an unusual woman who developed paranoid ideation, memory impairment, and progressive dementia at a psychiatry meeting in Tubingen. He demonstrated that her brain at autopsy exhibited hitherto undescribed abnormalities, he designated as neuritic plaques in the extracellular spaces, and neurofibrillary tangles within the neurons. He postulated that these led to neurodegeneration and cell death, producing dementia. His colleague Emile Kraepelin promptly called this “Alzheimer’s Disease”. Even after a century, research has not resulted in a cure in sight for this disabling ailment.
Identification of amyloid beta as the main constituent of plaques and phosphorylated tau as the tangle within neurons led to a rush to discover its biology. Patients with Alzheimer’s disease present to neurologists with memory impairment, changes in personality and behavior and at times impairment in linguistic abilities and visuo-spatial skills. Neurologists rely on imaging of the brain to elucidate regional shrinkage and subdued glucose utilization to correlate the clinical features.
Therapy attempts (using numerous methodologies) at blocking the accumulation of amyloid extracellularly and phosphorylation of tau intraneuronally have failed in clinical trials. Today, once Alzheimer’s disease has set in, therapy is essentially supportive. Drugs prescribed augment the failing production of a neurotransmitter called acetylcholine in the brain and attempt to slow down neural degeneration. Some medications are prescribed to control the behavioral aberrations that patients exhibit.
The current view is that multiple pathways lead to this catastrophic form of brain failure. It is accepted that both neural degeneration and regeneration occur daily, albeit in a fine balance.
A sedentary lifestyle, untreated diabetes and hypertension, poor sleep hygiene in middle life and sleep disorders like sleep apnea can accelerate the development of Alzheimer’s disease in a genetically vulnerable individual. Regular cardiovascular exercise, investment in a good sleep hygiene, a balanced diet rich in vegetables and fruits, an upbeat and enthusiastic outlook are all health investments that are pro-regeneration. Healthy social connectivity and pursuing novel hobbies/passions, and maintaining good oral hygiene are also neuro-protective.
The discovery of an exclusive sleep driven excretory system in the brain called the ‘Glymphatic system’ has resulted in an enthusiastic investigation of sleep as a novel biomarker of amyloid biology. The glymphatic system demonstrably excretes both amyloid and tau daily in normal individuals and even a few nights of sleep deprivation can tilt this balance unfavorably for the brain.
Therefore, sleep disorders like sleep apnea (characterized by sub-optimal sleep-related breathing) can act as a biological catalyst accelerating brain amyloid and tau accumulation. Maintaining disciplined sleep hygiene and the early treatment of sleep disorders may stave off the impending spectre of Alzheimer’s disease in later life.
Also read: Predicting Alzheimer’s is now possible, says study
Many a luminary with sterling careers in public domains have fallen prey to this occupational compulsion of sleep deprivation and gone on to develop Alzheimer’s disease. Names like Ronald Reagan, Margaret Thatcher, Agatha Christie, Charles Bronson, Omar Sharif, Rita Hayworth, and Sean Connery abound in the array of those who fell prey to this devastating degenerative disorder of late life. Clearly some of the byproducts of civilization, for example, dietary indulgence, sleep indiscipline, fragmentation of the social fabric of integrated families, and loneliness in late life, are the unrecognized predators lurking in the shadows of brain biology, ready to exact their ‘pound of brain’, despite the perceived heroics of modern medicine. One must pause and introspect.
Our lifestyles are due for a reformation and time may be running out for those in late middle life.
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